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Associations of autophagy with lung diffusion capacity and oxygen saturation in severe COPD: effects of particulate air pollution

Authors Lee K, Chiang L, Ho S, Liu W, Chen T, Feng P, Su C, Chuang K, Chang C, Chuang H

Received 22 March 2016

Accepted for publication 21 May 2016

Published 11 July 2016 Volume 2016:11(1) Pages 1569—1578

DOI https://doi.org/10.2147/COPD.S108993

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Charles Downs

Peer reviewer comments 3

Editor who approved publication: Dr Richard Russell


Kang-Yun Lee,1,2,* Ling-Ling Chiang,1,3,* Shu-Chuan Ho,1,3 Wen-Te Liu,1–3 Tzu-Tao Chen,1 Po-Hao Feng,1,2 Chien-Ling Su,1,3 Kai-Jen Chuang,4,5 Chih-Cheng Chang,1,2 Hsiao-Chi Chuang1–3

1Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, 2Department of Internal Medicine, School of Medicine, 3School of Respiratory Therapy, 4Department of Public Health, School of Medicine, College of Medicine, 5School of Public Health, College of Public Health and Nutrition, Taipei Medical University, Taipei City, Taiwan

*These authors contributed equally to this work

Abstract: Although traffic exposure has been associated with the development of COPD, the role of particulate matter <10 µm in aerodynamic diameter (PM10) in the pathogenesis of COPD is not yet fully understood. We assessed the 1-year effect of exposure to PM10 on the pathogenesis of COPD in a retrospective cohort study. We recruited 53 subjects with COPD stages III and IV and 15 healthy controls in a hospital in Taiwan. We estimated the 1-year annual mean levels of PM10 at all residential addresses of the cohort participants. Changes in PM10 for the 1-year averages in quintiles were related to diffusion capacity of the lung for carbon monoxide levels (r=−0.914, P=0.029), changes in the pulse oxygen saturation (ΔSaO2; r=−0.973, P=0.005), receptor for advanced glycation end-products (r=−0.881, P=0.048), interleukin-6 (r=0.986, P=0.002), ubiquitin (r=0.940, P=0.017), and beclin 1 (r=0.923, P=0.025) in COPD. Next, we observed that ubiquitin was correlated with ΔSaO2 (r=−0.374, P=0.019). Beclin 1 was associated with diffusion capacity of the lung for carbon monoxide (r=−0.362, P=0.028), ΔSaO2 (r=−0.354, P=0.032), and receptor for advanced glycation end-products (r=−0.471, P=0.004). Autophagy may be an important regulator of the PM10-related pathogenesis of COPD, which could cause deterioration in the lung diffusion capacity and oxygen saturation.

Keywords: 6-minute walk distance, air pollution, beclin 1, lung function, receptor for advanced glycation end-products

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